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G Piasecka

Publications and source records attributed to G Piasecka.

26 records · Page 2Linked to original sources
PubMed1990

Nicotine increases human polymorphonuclear leukocytes chemotactic response--a possible additional mechanism of lung injury in cigarette smokers.

Human polymorphonuclear leukocytes (PMNL) which are a potential source of proteolytic enzymes and reactive oxidant species contribute to the development of pulmonary emphysema in cigarette smokers. We found that nicotine at concentrations that occur in smokers' plasma enhances human PMNL chemotactic response to zymosan-activated serum (ZAS) and n-formyl-methionyl-leucyl-phenylalanine (FMLP). Maximal increase in chemotactic migration was at nicotine concentration 1 mumol/l. Higher concentrations, above 0.1 mmol/l inhibited PMNL chemotactic response and spontaneous migration. Nicotine also enhanced PMNL influx to the place of inflammation developed in the mouse pleural cavity after injection of ZAS. The number of PMNL found in the pleural cavity was 1.9-fold higher (p less than 0.001, n = 5) when animals were pretreated with 0.15 mg of nicotine. However, this drug itself (concentrations of 0.1 mumol/l to 10 mmol/l) had weak chemotactic activity for PMNL. It seems that the stimulatory action of nicotine on PMNL chemotaxis may be partly responsible for increased PMNL numbers in the lower airways of cigarette smokers and following formation of the elastase/antielastase imbalance in lung tissue.

Animals↗
PubMed1990

Chemotactic activity of histones for human polymorphonuclear leukocytes.

The chemotactic activity of histones for human polymorphonuclear leukocytes (PMNL) was investigated using the under-agarose method. Total histone and histone fractions H1, H2a, H2b, H3, H4 were prepared from calf thymus and dissolved in phosphate buffered saline (PBS) pH 7.4. At concentrations of 1 and 0.1 mg/ml all histone preparations were chemotactic for PMNL. The PMNL migration (expressed as a chemotactic index) to total histone (1 mg/ml) was 1.5 +/- 0.2 (n = 8) and to histone fractions it ranged from 1.2 to 1.4. The injection of total histone (50 micrograms) to the mouse pleural cavity induced cell influx. The mean PMNL number found in this cavity (0.33 +/- 0.15 X 10(6] was 3.6-fold higher in this group as compared to PBS-treated animals. Human PMNL during 60 min incubation with total histone (10 micrograms/ml) or with total histone and cytochalasin B (CB, 4.8 micrograms/ml) released 12.9 +/- 2.5 (n = 9) and 40.6 +/- 4.9 (n = 4) % of the total myeloperoxidase cell activity. Total histone (1 to 10 micrograms/ml) did not stimulate hydrogen peroxide generation independently of the presence of CB and had no influence on its production induced by phorbol myristate acetate. Our results suggest that histones released from cell debris in the place of inflammation could secondarily modulate to some extent its course by enhancing PMNL influx and their activation. These findings may be important for the course of inflammatory response in lungs especially in the light of their susceptibility to proteolytic injury.

Chemotaxis, Leukocyte↗
PubMed1990

DNA activates human polymorphonuclear leukocytes--a new importance of DNA presented in the inflammatory tracheobronchial secretion.

DNA from calf thymus (1 to 10 micrograms/ml) was shown to stimulate the release of myeloperoxidase (MPO) and low amounts of H2O2 (about 1.5 nmoles/10(6) cells) from human polymorphonuclear leukocytes (PMNL). PMNL during 60 min incubation with DNA (10 micrograms/ml) and with DNA and cytochalasin B (4.8 micrograms/ml) released 14.4 +/- 3.4 and 25.5 +/- 4.8% (n = 7) of the total MPO cell activity, respectively. Higher DNA concentrations (0.25 to 1mg/ml) were chemotactic for PMNL as assayed under agarose method. At DNA concentration 1mg/ml the chemotactic index reached 1.5 +/- 0.2 and was approximate to value 1.7 +/- 0.2 (n = 7) obtained with zymosan-activated serum. However, the introduction of DNA to the mouse pleural cavity caused insignificant increase in the number of PMNL and lymphocytes recovered from the cavity at 3 h after injection, comparing it to material obtained from buffer-treated animals. The yield of DNA preparation from purulent sputum (about 10 micrograms/ml) indicates that DNA concentrations which activate PMNL in vitro occur in the inflammatory tracheobronchial secretion. The DNA from sputum electrophoresed on the 0.6% agarose gel reveal pattern which could be the result of nucleosomal DNA degradation. These results suggest that DNA released from nuclear debris in the place of inflammation, especially in the lower respiratory tract could secondarily modulate its course by PMNL activation. This novel role of DNA may be important for pulmonary pathology since lungs are susceptible to proteolytic and oxidant mediated injury.

Animals↗
PubMed1989

Chemotactic activity of elastin-derived peptides for human polymorphonuclear leukocytes and their effect on hydrogen peroxide and myeloperoxidase release.

The chemotactic activity of elastin-derived peptides (EP) for human polymorphonuclear leukocytes (PMNL) was investigated using the under agarose method. The EP were produced by digesting the bovine ligament elastin with porcine pancreatic elastase. Thus prepared digest had weak chemotactic activity for PMNL. The mean chemotactic index for all tested EP concentrations did not exceed 1.30 and was lower than that obtained with zymosan-activated serum (ZAS, n-formyl-methionyl-leucyl-phenylalanine (FMLP) 2.2 +/- 0.40, 3.1 +/- 0.32, (n = 10) respectively. However, EP (50 micrograms) after injection to the mouse pleural cavity induced PMNL influx. The mean PMNL number found in this cavity was 0.09 +/- 0.03 x 10(6) for PBS and 0.18 +/- 0.03 +/- 10(6) for EP injection (p less than 0.01 n = 6). Human PMNL during 60 min incubation with EP (1 to 10 micrograms/ml) or with EP and cytochalasin B (CB 4.8 micrograms/ml) released myeloperoxidase and low amounts of hydrogen peroxide. At 1 micrograms/ml and in presence of CB elastin digest was nearly as active in myeloperoxidase release as FMLP (300 ng/ml). The values reached 17.1 +/- 2.5 and 19.7 +/- 2.1% of the total activity of whole cell lysate, respectively. The obtained results suggest that EP produced in vivo in the site of inflammation could modulate to some extent its course by enhancing PMNL influx and their activation. It seems that such mechanism of enhancement of the inflammatory response may occur in the lungs which are rich in elastin fibers.

Animals↗
PubMed1989

Ascorbic acid inhibits polymorphonuclear leukocytes influx to the place of inflammation--possible protection of lung from phagocyte-mediated injury.

Ascorbic acid as a scavenger of oxidants derived from human polymorphonuclear leukocytes (PMNL) may have clinical significance in antioxidant prevention of emphysema. However, there is a risk relevant to its administration because this drug was reported to enhance PMNL chemotactic response and thus could create protease burden in the lower airways. In this study we have investigated the effect of ascorbic acid on the PMNL influx to the place of inflammation developed in the mouse pleural cavity after injection of zymosan-activated serum (ZAS). We also evaluated the influence of ascorbic acid on human PMNL spontaneous migration, chemotaxis to ZAS and n-formyl-methionyl-leucyl-phenylalanine (FMLP) under agarose. The previous ascorbic acid intraperitoneal administration (single dose 10 mg per day for 3 following days) inhibited leukocyte influx. Total number of cells found in the cavity, number of PMNL and lymphocytes was 2.4, 3.5, 1.7-fold lower than in animals without ascorbic acid, respectively. In vitro ascorbic acid (concentrations of 1 to 10 mg/dl) enhanced PMNL spontaneous migration, concentrations 10 mg/dl and higher inhibited PMNL chemotaxis to ZAS and had no influence on migration of the cells toward FMLP. These results suggest that ascorbic acid may be useful for prevention of lung oxidant injury not only as oxidant scavenger but also as an inhibitor of PMNL influx to the pulmonary tissue.

Animals↗
PubMedDate not supplied

Ascorbic acid did not alter the content of conjugated dienes and malondialdehyde in organs of mice.

The aim of this study was to explore whether ip administration of ascorbic acid (AA) in a dose of 500 mg/kg, once a day for 3 following days, affected the content of lipid peroxidation products: malondialdehyde (MDA) and conjugated dienes (CD) in organs of mice. Injection of AA caused 2.1-, 1.3- and 1.8-fold increase in the concentration of this vitamin in liver, spleen and lungs, respectively, while the content of MDA and CD in these organs did not differ from values found in animals treated with 0.9% NaCl. It suggests that in our animal model AA did not act as a prooxidant enhancing the lipid peroxidation in various tissues.

Animals↗
PubMedDate not supplied

Ambroxol inhibits endotoxin-induced lipid peroxidation in mice.

Administration of ambroxol (70 mg/kg ip) once a day for 3 days protected lung and heart lipids from lipopolysaccharide (LPS, 17 mg/kg)-induced oxidative stress in mice. Ambroxol as a lipid peroxidation inhibitor was almost as active as an equivalent dose of N-acetylcysteine (27.6 mg/kg), a well known antioxidant. The lung and heart levels of conjugated dienes in animals pretreated with ambroxol were 3.3- and 1.7-times lower (p < 0.05 and p < 0.01) than those observed in the control group which received only buffer and subsequently LPS. These results indicate that ambroxol can sufficiently inhibit the harmful process of lipid peroxidation in vivo.

Ambroxol↗